کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9142070 | 1163895 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Monocytes promote natural killer cell interferon gamma production in response to the endogenous danger signal HMGB1
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کلمات کلیدی
HMGB1inflammation - التهاب( توروم) Tumor immunology - ایمونولوژی تومورinterleukin-12 - اینترلوکین -12Interleukin-2 - اینترلوکین-۲NK cells - سلولهای NKtumor necrosis factor - فاکتور نکروز تومورMacrophages - ماکروفاژها،درشت خوارهاMonocytes - مونوسیتهاNecrosis - نکروز یا بافتمردگیInterferon gamma - گاما اینترفرون
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Monocytes promote natural killer cell interferon gamma production in response to the endogenous danger signal HMGB1 Monocytes promote natural killer cell interferon gamma production in response to the endogenous danger signal HMGB1](/preview/png/9142070.png)
چکیده انگلیسی
Substantial attention has been paid to the role of the toll-like receptor (TLR) ligands of late and their role in regulating the innate immune response. They serve as exogenous danger signals important in informing and driving the distal adaptive immune response to pathogens. Less clear has been the role of the nominal endogenous danger signals released and recognized in stressed cells following genotoxic or metabolic stress as occurs in progressively growing tumors. HMGB1 (high-mobility group B1) is a nuclear protein well characterized for its ability to modify DNA access to transcriptional proteins that is released from necrotic cells as well as secreted through the endosomal route from hematopoietic cells, serving as a late mediator of sepsis. It interacts with high-affinity RAGE (receptor for advanced glycation end products) and TLR2 receptors. Here we show that HMGB1 enhances interferon gamma release from macrophage (but not dendritic cell)-stimulated NK cells. This is effective only when coupled with other pro-inflammatory cytokines particularly with IL-2 in combination with IL-1 or IL-12. We have used this information to suggest that HMGB1, which also promotes epithelial migration and proliferation, drives repair in the absence or inhibition of other factors but enhances inflammation in their presence. The implications for tumorigenesis and tumor progression are quite important as they may be for other states of chronic inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 42, Issue 4, February 2005, Pages 433-444
Journal: Molecular Immunology - Volume 42, Issue 4, February 2005, Pages 433-444
نویسندگان
Richard A. DeMarco, Mitchell P. Fink, Michael T. Lotze,